text: Three different types of β-adrenergic receptors have been identified by molecular pharmacology. β1-receptors are located in the heart and consist of about 75% of all β-receptors. β2-receptors can be found in the smooth muscles of vessels and the bronchies. β3-receptors are presumed to be involved in fatty acid metabolism and are found in the adipocytes. β-blockers cause a competitive inhibition of the β-receptor, which counters the effects of catecholamines. β1 and β2-receptors are G-protein coupled receptors, which couple to Gαs-proteins. When activated, it stimulates an increase in intracellular cAMP via the adenylyl cyclase. cAMP, which is the second messenger, then activates protein kinase A that phosphorylates the membrane's calcium channel and increases the entry of calcium into the cytosol. Protein kinase A also increases the release of calcium from the sarcoplasmic reticulum, which causes a positive inotropic effect. The phosphorylation of troponin I and phospholamban by protein kinase A causes the lusitropic effects of β-blockers. This increases the re-uptake of calcium by the sarcoplasmic reticulum.
  β-blockers are sympatholytic drugs. Some β-blockers partially activate the receptor while preventing catecholamines from binding to the receptor, making them partial agonists. They provide a background of sympathetic activity, while preventing normal and enhanced sympathetic activity. These β-blockers possess intrinsic sympathomimetic activity (ISA). Some of them also possess what is called membrane-stabilizing activity (MSA) on myocardial muscle fibers.